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PLoS One. 2015 May 26;10(5):e0126926. doi: 10.1371/journal.pone.0126926. eCollection 2015.

Environmental mold and mycotoxin exposures elicit specific cytokine and chemokine responses.

Author information

1
Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of America; Institute for Liberal Arts, Emerson College, Boston, MA, United States of America.
2
Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of America; Hebrew Senior Life Institute for Aging Research and Harvard Medical School, Boston, MA, United States of America; Broad Institute of MIT and Harvard, Cambridge, MA, United States of America.
3
Research Resources Center, University of Illinois at Chicago, Chicago, IL, United States of America.
4
Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States of America.
5
Institute for Health Informatics, University of Minnesota School of Nursing, Minneapolis, MN, United States of America.
6
Department of Medicine, University of Illinois College of Medicine, Chicago, IL, United States of America.

Abstract

BACKGROUND:

Molds can cause respiratory symptoms and asthma. We sought to use isolated peripheral blood mononuclear cells (PBMCs) to understand changes in cytokine and chemokine levels in response to mold and mycotoxin exposures and to link these levels with respiratory symptoms in humans. We did this by utilizing an ex vivo assay approach to differentiate mold-exposed patients and unexposed controls. While circulating plasma chemokine and cytokine levels from these two groups might be similar, we hypothesized that by challenging their isolated white blood cells with mold or mold extracts, we would see a differential chemokine and cytokine release.

METHODS AND FINDINGS:

Peripheral blood mononuclear cells (PBMCs) were isolated from blood from 33 patients with a history of mold exposures and from 17 controls. Cultured PBMCs were incubated with the most prominent Stachybotrys chartarum mycotoxin, satratoxin G, or with aqueous mold extract, ionomycin, or media, each with or without PMA. Additional PBMCs were exposed to spores of Aspergillus niger, Cladosporium herbarum and Penicillium chrysogenum. After 18 hours, cytokines and chemokines released into the culture medium were measured by multiplex assay. Clinical histories, physical examinations and pulmonary function tests were also conducted. After ex vivo PBMC exposures to molds or mycotoxins, the chemokine and cytokine profiles from patients with a history of mold exposure were significantly different from those of unexposed controls. In contrast, biomarker profiles from cells exposed to media alone showed no difference between the patients and controls.

CONCLUSIONS:

These findings demonstrate that chronic mold exposures induced changes in inflammatory and immune system responses to specific mold and mycotoxin challenges. These responses can differentiate mold-exposed patients from unexposed controls. This strategy may be a powerful approach to document immune system responsiveness to molds and other inflammation-inducing environmental agents.

PMID:
26010737
PMCID:
PMC4444319
DOI:
10.1371/journal.pone.0126926
[Indexed for MEDLINE]
Free PMC Article

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